ArticleJournal of virology2002
Expression of transcription factor AML-2 (RUNX3, CBF(alpha)-3) is induced by Epstein-Barr virus EBNA-2 and correlates with the B-cell activation phenotype.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 76 citations in OpenAlex.
- Single-Cell Transcriptomic Profiling Identifies B Cell-Intrinsic Dysregulation of Sphingolipid Biosynthesis and Could Be Improved by Inhibiting UGCG in Primary Immune Thrombocytopenia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- BAF complexes maintain accessibility at stimulus-responsive chromatin and are required for transcriptional stimulus responses.bioRxiv : the preprint server for biology · 2026Article
- Article
- Runt-related transcription factors in human carcinogenesis: a friend or foe?Journal of cancer research and clinical oncology · 2023Review
- Epstein-Barr virus perpetuates B cell germinal center dynamics and generation of autoimmune-associated phenotypesFrontiers in immunology · 2022Article
- Super-enhancers for RUNX3 are required for cell proliferation in EBV-infected B cell lines.Gene · 2021Article
- Article
- Interleukin 16 contributes to gammaherpesvirus pathogenesis by inhibiting viral reactivation.PLoS pathogens · 2020Article
- The Neat Dance of COVID-19: NEAT1, DANCR, and Co-Modulated Cholinergic RNAs Link to Inflammation.Frontiers in immunology · 2020Article
- Investigating the effect of dependence between conditions with Bayesian Linear Mixed Models for motif activity analysis.PloS one · 2020Article
- RUNX family: Oncogenes or tumor suppressors (Review).Oncology reports · 2019Review
- LTRs activated by Epstein-Barr virus-induced transformation of B cells alter the transcriptome.Genome research · 2018Article
- A B Cell Regulome Links Notch to Downstream Oncogenic Pathways in Small B Cell Lymphomas.Cell reports · 2017Article
- Core binding factor (CBF) is required for Epstein-Barr virus EBNA3 proteins to regulate target gene expression.Nucleic acids research · 2017Article
- Article
- RUNX super-enhancer control through the Notch pathway by Epstein-Barr virus transcription factors regulates B cell growth.Nucleic acids research · 2016Article
- IGHV1-69 polymorphism modulates anti-influenza antibody repertoires, correlates with IGHV utilization shifts and varies by ethnicity.Scientific reports · 2016Article
- The RUNX complex: reaching beyond haematopoiesis into immunity.Immunology · 2015Review
- Article
- Repression of the proapoptotic cellular BIK/NBK gene by Epstein-Barr virus antagonizes transforming growth factor β1-induced B-cell apoptosis.Journal of virology · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To identify cell proteins regulated by the Epstein-Barr virus (EBV) transcription factor EBNA-2, we analyzed a cell line with conditional EBNA-2 activity by using microarray expression profiling. This led to the identification of two novel target genes induced by EBNA-2. The first of these, interleukin-16, is an immunomodulatory cytokine involved in the regulation of CD4 T cells. The second, AML-2, is a member of the Runt domain family of transcription factors. Quiescent B cells initially expressed AML-1 but, 48 h after virus infection, the levels of AML-1 decreased dramatically, whereas the amount of AML-2 protein increased. Analysis of a panel of B-cell lines indicated that AML-2 expression is normally predominant in EBV latency III, whereas AML-1 is associated with EBV latency I or EBV-negative cells. The AML genes are the first example of cell transcription factors whose expression correlates with the latency I/III phenotype.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.